Abstract
We investigated the possibility that the effects of propofol on sarcoplasmic reticulum (SR) function may contribute to the myocardial depression induced by this anesthetic. With guinea pig isolated papillary muscles, the effects of propofol on transient alterations in contractility (termed "potentiated-state" contractions), after abrupt changes in stimulation frequency and brief periods of rest, were compared with those of enflurane and the inhibitor of SR function, ryanodine. These potentiated-state contractions are mediated by calcium derived largely from the SR. Propofol, enflurane, and ryanodine were applied at concentrations that produced approximately 50%-60% inhibition of "steady-state" contraction. Ryanodine abolished and enflurane attenuated the potentiated-state contractions, whereas propofol had no apparent effect. Although impairment of SR function may contribute to the depression of contractility induced by enflurane, propofol has no major effect on SR function.
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